Expression of the Mxra8 Receptor Promotes Alphavirus Infection and Pathogenesis in Mice and Drosophila.
Alphavirus
/ drug effects
Animals
Antibodies, Monoclonal
/ pharmacology
Arthritis
/ pathology
CRISPR-Cas Systems
/ genetics
Chikungunya Fever
/ metabolism
Chikungunya virus
/ drug effects
Drosophila Proteins
/ metabolism
Drosophila melanogaster
/ drug effects
Immunoglobulins
/ deficiency
Inflammation
/ pathology
Membrane Proteins
/ deficiency
Mice, Inbred C57BL
Mutation
/ genetics
alphavirus
arthritis
mice
pathogenesis
receptor
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
03 09 2019
03 09 2019
Historique:
received:
09
05
2019
revised:
18
07
2019
accepted:
29
07
2019
entrez:
5
9
2019
pubmed:
5
9
2019
medline:
15
9
2020
Statut:
ppublish
Résumé
Mxra8 is a recently described receptor for multiple alphaviruses, including Chikungunya (CHIKV), Mayaro (MAYV), Ross River (RRV), and O'nyong nyong (ONNV) viruses. To determine its role in pathogenesis, we generated mice with mutant Mxra8 alleles: an 8-nucleotide deletion that produces a truncated, soluble form (Mxra8
Identifiants
pubmed: 31484075
pii: S2211-1247(19)31021-6
doi: 10.1016/j.celrep.2019.07.105
pmc: PMC6745702
mid: NIHMS1539073
pii:
doi:
Substances chimiques
Antibodies, Monoclonal
0
Drosophila Proteins
0
Immunoglobulins
0
Membrane Proteins
0
Mxra8 protein, mouse
0
Types de publication
Case Reports
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
2647-2658.e5Subventions
Organisme : NIAID NIH HHS
ID : R01 AI123348
Pays : United States
Organisme : NIAMS NIH HHS
ID : P30 AR073752
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI095436
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI143673
Pays : United States
Organisme : NIAID NIH HHS
ID : T32 AI007163
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI114816
Pays : United States
Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
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